Accessibility navigation


The stimulation of mitogenic signaling pathways by N-POMC peptides

Pepper, D. J. and Bicknell, A. B. (2009) The stimulation of mitogenic signaling pathways by N-POMC peptides. Molecular and Cellular Endocrinology, 300 (1-2). pp. 77-82. ISSN 0303-7207

Full text not archived in this repository.

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

To link to this item DOI: 10.1016/j.mce.2008.09.021

Abstract/Summary

The N-terminal fragment of pro-opiomelancortin (POMC) has been shown previously to act as an adrenal mitogen. However, little is known about the molecular mechanisms by which mitogenesis is stimulated, although it has been shown that N-POMC1-28 Stimulates the ERK pathway in human H295R cells. We have investigated signaling stimulated by N-POMC1-28 and N-POMC1-49 in the mouse Y1 cell line and found that both peptides stimulate ERK phosphorylation with maximal stimulation being achieved within 5 min. Similar results were observed for both MEK and c-Raf phosphorylation, although N-POMC1-49 stimulated the phosphorylation of Akt more robustly than N-POMC1-28. We also investigated the expression of tyrosine kinase receptors in adrenal cells. PCR utilizing degenerate primers was performed on cDNA from both Y1 cells and rat adrenal tissue. Sequencing of 114 clones from each cDNA population revealed the expression of a number of receptors, several of which have not been described previously in the adrenal. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

Item Type:Article
Refereed:Yes
Divisions:Life Sciences > School of Biological Sciences
ID Code:9674
Uncontrolled Keywords:Adrenal, PoMC, N-POMC, ERK, AKT, Receptor tyrosine kinase, ADRENOCORTICAL TUMOR-CELLS, RECEPTOR TYROSINE KINASE, ADRENAL GROWTH, PROOPIOMELANOCORTIN, INHIBITION, PITUITARY, HORMONE, RYK, AXL, MONOPHOSPHATE

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation